ung cancer patients given amrubicin (Calsed) as a second-line treatment had a significantly improved response rate and longer progression-free survival than patients treated with topotecan (Hycamtin), as per research presented at the 14th World Conference on Lung Cancer in Amsterdam, hosted by the International Association for the Study of Lung Cancer (IASLC).
"Amrubicin showed significant improvements in tumor shrinkage, symptom control and progression-free survival over topotecan without improving overall survival, the primary endpoint of the trial," said principal investigator Dr. Joachim von Pawel, of the Asklepios Hospital Munich-Gauting in Gera number of. "However, for patients with the most difficult-to-treat small cell lung cancer, amrubicin offered an improvement in overall survival compared with topotecan."
Second-line therapy is given to patients after the initial, or first-line, therapy has failed.
In the study, 637 patients were randomized to amrubicin or to topotecan. Patients on amrubicin reported better symptom control and quality of life (Lung Cancer Symptom Scale 0.2 vs 5.6 and LCSS-SB -0.1 vs 5.2 for amrubicin and topotecan, respectively). They also reported fewer adverse events, including neutropenia (41% vs 53% for the topotecan arm), thrombocytopenia (21% vs 54%), anemia (16% vs 30%), infections (16% vs 10%), febrile neutropenia (10% vs 4%), all P<0.05, and cardiac disorders (5% vs 5%; P=0.84).........
Thalidomide has shown potential to be used as the first adjuvant treatment for hepatocellular carcinoma (HCC), as per data presented at the International Liver CongressTM 2011.1.
A newly released study found thalidomide gave HCC patients who'd undergone grossly curative resection surgical removal of the malignant part of the liver double the two-year disease free survival rate (65%) in comparison to placebo (33%).
However, the study did find that the two-year overall survival rate was comparable between patients treated with thalidomide and patients given placebo � 84.2% and 85.7% respectively.
Daniele Prati, EASL's Scientific Committee Member and Press Committee Chairman, commented: "Current options for adjuvant treatment in HCC are very limited and clinical trial results have been disappointing. Thalidomide has already been proven to work well in many other areas and this study shows it could potentially benefit HCC patients who are especially difficult to treat. Overall, it is important to continue research in evaluating adjuvant treatment in HCC".
Surgery is the main form of therapy for HCC, but is only possible for a small proportion of those afflicted. Even after curative resection, recurrence is common and is the main cause of death. Adjuvant treatment that is, chemotherapy after surgery � is thus attempted to try to improve outcomes.2.........
Digoxin may be a possible treatment for prostate cancer
Researchers have identified digoxin as a possible treatment for prostate cancer, using a combination of laboratory science and epidemiology that is unprecedented in its cooperative nature.
"Epidemiologists and basic researchers often do not understand each other, as we often are only clear on our own strengths and the other's weaknesses," said Elizabeth Platz, Sc.D., M.P.H, professor of epidemiology and the Martin D. Abeloff, M.D., scholar in cancer prevention at Johns Hopkins University.
For the current paper, published in Cancer Discovery, the newest journal of the American Association for Cancer Research, which will debut at the AACR 102nd Annual Meeting 2011, Platz shares authorship with Srinivasan Yegnasubramanian, M.D., Ph.D., assistant professor of oncology at Johns Hopkins. Platz said the multidisciplinary team of researchers had come together to identify existing drugs that could be used to treat prostate cancer in a process called drug repositioning.
"If you use drugs that are already available then you have a long history of safety research that does not necessarily need to be redone, and we can move more quickly to testing whether the drug will actually work in a new setting," said Platz.
The idea of drug repositioning has been offered before, but each branch of scientific inquiry had enough flaws that it had not previously gained substantial traction. "When we combined the basic science and the epidemiology approaches, the flaws were not the same and were covered by their respective strengths," she said.........
Scientists have observed that it may not be necessary to look for tumors directly in prostate cancer patients � analyzing non-tumor tissue appears to be an effective option, as per study results published in Cancer Research, a journal of the American Association for Cancer Research.
"A biopsy needle does not need to hit a tumor to detect the presence of tumor," said lead researcher Dan Mercola, M.D., Ph.D., professor of pathology and laboratory medicine at the University of California at Irvine. "It is reminiscent of the game Battleship; we can detect more cancer cases using 12 shots with a biopsy needle than would otherwise be the case because we have made the ships bigger".
More than 1 million prostate biopsies are performed in the United States each year, and these diagnostic tests can miss up to 30 percent of clinically significant prostate cancers. As a number of as one third of patients receive repeat biopsies within a year due to equivocal first results, Mercola said. Based on these study results, physicians could possibly detect changes in non-tumor tissue that indicate a tumor appears to be present, which could allow patients to be given a follow-up biopsy sooner.
"Changes in the non-tumor tissue surrounding the tumor have long been considered to be important to tumor growth. Interfering with this process could have therapeutic value," he said. "The information in non-tumor tissue indicating 'presence of tumor' or not indicates who needs urgent re-biopsy and allows patients to consider alternative therapies to surgery or radiation such as neoadjuvant treatment or prostate cancer prevention therapy".........
rotein that protects cancer cells from chemo and radiation
Research led by Daitoku Sakamuro, PhD, Assistant Professor of Pathology at LSU Health Sciences Center New Orleans and the LSUHSC Stanley S. Scott Cancer Center, has identified a protein that enables the activation of a DNA-repair enzyme that protects cancer cells from catastrophic damage caused by chemo and radiation treatment. This protein, called c-MYC oncoprotein, can initiate and promote almost all human cancers and discovering the role it plays in cancer therapy resistance may lead to advances that save lives. The work is reported in the March 29, 2011 issue of Science Signaling, a publication of the American Association for the Advancement of Science. Eventhough researchers have known that cancer cells can acquire resistance to DNA-damaging therapeutic agents, the genetic mechanisms through which this occurs have remained unclear until now.
Using the chemotherapy drug, cisplatin (which is usually used as a first-line treatment for various cancers) to design a set of experiments, the research team observed that the c-MYC oncoprotein increases cisplatin resistance by decreasing production of a c-MYC inhibitor called BIN1. BIN1 suppressed an enzyme essential for DNA repair, and the sensitivity of cancer cells to cisplatin depended upon BIN1 abundance. Overproducing the c-MYC oncoprotein repressed BIN1, blocking its life-saving action.........
newly released study suggests that combining two experimental anticancer peptide agents might simultaneously block formation of new tumor blood vessels while also inhibiting the growth of tumor cells.
This early test of the two agents in a breast cancer model suggests that the double hit can stifle tumor progression, avoid drug resistance and cause few side effects, say scientists at the Ohio State University Comprehensive Cancer Center - Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC - James) who developed the agents and reviewed their effectiveness in laboratory and animal tests.
The researchers designed one of the agents to prevent human epithelial growth factor from interacting with HER-2, a molecule that marks a especially aggressive form of breast cancer. The other inhibitor blocks the action of vascular endothelial growth factor (VEGF), which stimulates the growth of new blood vessels that tumors need to grow beyond a certain size.
The findings are described in two papers published online in the Journal of Biological Chemistry. One presents the development of a novel VEGF inhibitor; the other describes the HER-2 inhibitor and the preclinical testing of the two agents together.
"When we combined our peptide HER-2 inhibitor with the VEGF peptide that inhibits angiogenesis, we observed significant additive benefits in reducing tumor burdens in preclinical studies," says principal investigator Pravin Kaumaya, professor of obstetrics and gynecology, of molecular and cellular biochemistry, and of microbiology, and director of the division of vaccine development at the OSUCCC - James.........
Scientists at UT Southwestern Medical Center have identified a chemical compound that may eventually lead to a drug that fights cancers that are dependent on a particular anti-viral enzyme for growth.
The scientists are testing the compound's effectiveness at fighting tumors in mice. If it is successful, they will then work to develop a drug based on the compound to combat pancreatic and non-small cell lung cancer, two cancer types in which this particular enzyme, TBK-1, often is mandatory for cancer cell survival.
"Our prediction is that TBK-1 is a good pharmacological intervention target for a subset of lung and pancreatic cancers that are addicted to the activity of this enzyme. We believe there is a large population of cancer patients that could respond to inhibition of this activity," said Dr. Michael White, professor of cell biology and senior author of the study in the Feb. 18 issue of Molecular Cell.
The investigation, which lasted three and a half years, revealed how activation of the natural virus-fighting protein TBK-1 is hijacked in cancer cells to support growth and survival.
More than 250,000 compounds were screened to find one that would inhibit the enzyme's cancer-protection mechanism. The most effective, a compound called 6-aminopyrazolopyrimidine developed in collaboration with pharmaceutical company Amgen, blocked TBK-1's effects in 40 percent to 50 percent of the non-small cell lung cancer and pancreas cancer tissue cultures tested, reducing cancer growth. TBK-1 is activated by the Ras family of oncogenes, which are mutated in 40 percent of lung cancers and 90 percent of pancreas cancers.........
Paul Doetsch, PhD, of Emory University partnered with Damien Bregeon, PhD, of Institut de Genetique et Microbiologie in Paris on an article published in the March 2011 issue of Nature Reviews Cancer.
DNA provides the instruction manual for all life forms. Occasionally, instructions are not carried out properly, and bad messages are sent leading to the creation of mutant proteins and possible tumor development.
Paul Doetsch, PhD, professor of radiation oncology and biochemistry and associate director for basic research at Emory's Winship Cancer Institute and Damien Bregeon, PhD, at Institut de Genetique et Microbiologie in Paris, have outlined the role this process - known as transcriptional mutagenesis - might play in tumor development in a Nature Reviews Cancer article published online February 24th and in the March 2011 print edition.
"The majority of human cells do not multiply continuously but are slow-replicating and devote a large part of their energy to transcription," say the authors. "DNA damage can miscode at the damaged site and produce mutant transcripts. This process is transcriptional mutagenesis and could lead to the production of mutant proteins and may therefore be important in tumor development".
Transcriptional mutagenesis occurs when cells with damaged DNA produce bad messages during transcription, which leads to the creation of mutant proteins. Researchers already have learned that some genetic damages may block the transcription process, which is a signal for DNA repair molecules to move in and correct the mistake. When certain types of DNA damage are present, however, the non-dividing cells are capable of continuing transcription through the damage despite the erroneous coding messages. This problem can be exacerbated when cells have defects for repairing DNA damage.........
Prostate Cancer Treatment Is Different For Everyone
Prostate cancer is always a very scary diagnosis and one that many men do not know exactly what to do with. There are some ways that you can look at prostate cancer treatment and determine your course of treatment. Looking at the treatments that have proven to be the most successful can help you determine where you are going to go next.
Exploring all of the treatment options can help you to discover what is available for your treatment. There are combinations of treatment that could be recommended and this might work best for your particular situation. Cancer can spread to many parts of the body and you want to make sure that you are treating this cancer as early as possible to prevent this spread.
Radiation and chemotherapy are often treatments that occur upon the initial diagnosis. If this is a course of treatment you are considering, it can help to eradicate your cancer, but anyone with cancer normally understands there is no cure for cancer and treating problems as they arise is normally the only option.
Surgery is something that can be recommended for prostate cancer. This can require the complete or partial removal of the prostate and this can be a surgery that helps remove a large portion of the cancer. If your doctor recommends surgery as your treatment, you will want to completely understand what is involved in your particular surgery.
Surgery can also require a period of recovery and you want to understand your limitations and when you can return to more of a normal life. This will help you to get the most out of your recovery and you will not over do it in the beginning. Once you are fully recovered, your surgery may be a distant memory and you will be ready to move on with your life.
Alternative treatments are something that people suffering with cancer are checking into. It can be a great idea to combine alternative treatments with doctor recommended treatment and you will be able to relieve any pain you will be experiencing and all of your treatment will not come from only a traditional medicine source.
Prostate cancer treatment is something that is mufti-faceted. There is not just one treatment option and you will work closely with your doctor to come up with a plan that is right for your situation. This can help you to treat your prostate cancer and get on with your life.
"Profiling" To Detect Abnormalities: Including Cancer
An Ohio State University mathematician and colleagues are finding ways to tell the difference between healthy cells and abnormal cells, such as cancer cells, based on the way the cells look and move.
They are creating mathematical equations that describe the shape and motion of single cells for laboratory analysis.
Though this research is in its early stages, it represents an entirely new way of identifying cell abnormalities, including cancer. It could one day be useful in gauging future stages of a disease -- for example, by detecting whether cancer cells are aggressive and likely to spread throughout the body, or metastasize.
In a paper published online in the Bulletin of Mathematical Biology, scientists describe a mathematical model which analyzes image sequences of single, live cells to determine abnormalities manifested in their shape and behavior. A brain tumor cell was one of the cell types they analyzed in the study.
Huseyin Coskun, visiting assistant professor of mathematics at Ohio State and leader of the project, described their novel approach as a first step toward developing mathematical tools for diagnosing cell abnormalities and for giving potential prognoses.
Because the technique would allow doctors to view how cancer cells behave under different physical or chemical conditions, it could also be used to test different therapy strategies for each individual patient -- such as determining the most efficient dose of chemotherapeutic agents or radiation -- or even to test entirely new therapys.........
Why PSA levels reflect prostate cancer progression
Scientists at the Duke Cancer Institute who have been studying prostate cancer cells for decades now think they know why PSA (prostate-specific antigen) levels reflect cancer progression.
"This is the first demonstration of a mechanism that explains why PSA is a bad thing for a tumor to produce," said senior author Sal Pizzo, M.D., Ph.D., chair of the Duke Department of Pathology. "I am willing to bet there is also a connection in malignant cell growth with this particular biological signaling mechanism happening in other types of cells".
Using human prostate cancer cells in a laboratory culture, the team observed that an antibody reacts with a cell surface receptor called GRP78 on the cancer cells to produce more PSA. The PSA arises inside of the cancer cell and then moves outside of the cell, where it can bind with the same antibody, called alpha2-macroglobulin (α2M).
The PSA forms a complex with the antibody that also binds to the GRP78 receptor, and that activates several key pathways which stimulate cancer cell growth and cell movement and block cell death.
The study bolsters the case for measuring PSA as a marker of tumor progression, as well as for monitoring for α2M antibody levels.
"The use of PSA to make the initial diagnosis of prostate cancer has become controversial over the past decade," Pizzo said. "I personally believe PSA is more useful as a progression marker, especially with a baseline value on record at the time of the original treatment. A rapidly rising value and/or a very high value is reason for concern. I also think that monitoring the serum for the appearance of antibodies directed against GRP78 is also a good marker of progression".........
Neil Terry, left, and Adam Wax with a prototype of the new device.
Credit: Duke University Photography
A tiny light source and sensors at the end of an endoscope may provide a more accurate way to identify pre-malignant cells in the lining of the esophagus.
Developed by biomedical engineers at Duke University and successfully tested on patients during a clinical trial at the University of North Carolina at Chapel Hill, the device holds the promise of being a less invasive method for testing patients suspected of having Barrett's esophagus, a change in the lining of the esophagus due to acid reflux. Acid reflux occurs when stomach acid splashes, or refluxes, up into the esophagus.
Long periods of acid reflux can change the cells that line the esophagus, making them appear more like intestinal cells than esophageal cells. These cellular changes can also be a precursor to cancer. As in most cancers, early identification of these pre-malignant cells often leads to better outcomes for patients. Barrett's esophagus afflicts more than one percent of the U.S. population, with most patients above the age of 50.
Using an endoscope to reach the esophagus via the nose, physicians shine short bursts of this light at locations of suspected disease and sensors capture and analyze the light as it is reflected back. In particular, they are trying to spot characteristic changes within the layer of cells known as the epithelium, which line cavities and surfaces throughout the body.........
The immune system response in Drosophila to a wasp infection (above) is highly restrained, resulting in a thin layer of blood cells encapsulating the egg. However, blood cancer occurs (below) when there is an out-of-control response to a chronic inflammation, with a much thicker layer of red blood cells
Tiny parasitoid wasps can play an important role in controlling the populations of other insect species by laying their eggs inside the larvae of these species. A newly hatched wasp gradually eats the host alive and takes over its body.
The host insect is far from defenseless, however. In Drosophila (fruit flies), larvae activate humoral immunity in the fat body and mount a robust cellular response that encapsulates and chokes off the wasp egg.
New research by Dr. Shubha Govind, professor of biology at The City College of New York, and his colleagues reveals parallels between how this mechanism fights the wasp infection and the way blood cancer develops. "There are fundamental similarities in the processes," she explains. "The response to wasp infection is similar to acute inflammation while the cancer is akin to chronic inflammation in mammals, where regulation of the response to an infection also goes out of control".
Professor Govind reports that the immune system that counters wasp egg infection is highly restrained. The system works like a thermostat, with certain proteins detecting the infection and triggering the immune reactions. Once the egg has been destroyed the immune reactions come to a halt.
However, when the regulating mechanism goes haywire, cancer can develop. Through sumoylation, the correct balance between positive and negative factors is achieved, Professor Govind and his colleagues report.........
diagnosis of breast cancer and the fight that follows often represent a highly emotional, challenging time for a number of women and their families. In particular, medical procedures such as mastectomy (removal of a breast) can shake a woman's most basic sense of identity and leave equally devastating emotional scars. As part of the rebuilding process, a number of women elect to undergo breast reconstruction surgery. Performed by a plastic surgeon, this procedure returns the breast to a similar shape, size, and look (e.g., the nipple and areola can also be reconstructed). Some women choose to have the surgery immediately after the mastectomy whereas others wait until radiation treatment has been completed. Eventhough there are a number of reasons why women decide to have breast reconstruction, it is important to thoroughly weigh the risks and benefits with your physician-including when to have surgery, what type of procedure to select, and which implant if applicable-as far in advance as possible.
Breast reconstructive procedures fall into two categories: tissue flap or implant surgeries. There are advantages and disadvantages to each type of procedure. In tissue flap procedures, muscle, skin, and other tissue appears to be removed from other areas of the body (e.g., thighs, upper back, buttocks, or belly areas) and relocated to the chest area to recreate the breast(s). By contrast, implant reconstruction uses saline or gel implants in one or more surgeries to return the breast to the size and contour it previously had. Reconstruction of the nipple and areola often occur after breast reconstruction has been completed and the patient has had a few months of recovery time; this type of reconstruction may not be necessary if the mastectomy used a nipple-sparing procedure.........
Results for testing breast tumors for HER2 (http://www.mayoclinic.com/health/breast-cancer/AN00495) proteins and genes is most often straightforward when one piece of tumor (a single tumor block) is analyzed. However, tumors can be diverse, and scientists at Mayo Clinic (http://www.mayoclinic.org/) observed that HER2 results can vary in up to 10 percent of patients when several tumor blocks are analyzed.
This could have significant implications for patient therapy, say the researchers, who are presenting their findings at the 33rd Annual CTRC-AACR San Antonio Breast Cancer Symposium (http://www.sabcs.org/).
In their study, the scientists observed that while three independent teams of expert pathologists agreed most of the time on how slices from a single tumor block from a patient should be classified in terms of HER2 genes and proteins, a consensus was harder to reach when several blocks from the same patient were available for analysis.
In fact, the pathologists, from central laboratories at Mayo Clinic, the University of Southern California, and the University of Pittsburgh, found significant heterogeneity, or variability, between two tumor blocks taken from the same patient in 5 to 10 percent of cases. Most often, one tumor block showed a normal HER2 expression, while the second piece of tumor tested HER2+.........
Depression drug may relieve pain from breast cancer treatment
drug usually used to treat depression and anxiety disorder was effective at reducing joint and muscle pain linked to a breast cancer therapy, as per a research studyfrom the University of Michigan Comprehensive Cancer Center.
The women in the study were taking aromatase inhibitors, a type of drug designed to block the production of estrogen, which fuels some breast cancers. About half of women taking these drugs experience aches and pains in their joints and muscles that cannot be adequately relieved by over-the-counter painkillers. Up to 20 percent of these women will stop taking an aromatase inhibitor because of this pain.
"Since women typically take these drugs for five years, it is important that the side effects not interfere too much with their quality of life, or they will be less likely to continue taking the medicine, which may lead to a greater chance of their breast cancer returning," says study author N. Lynn Henry, M.D., Ph.D., assistant professor of internal medicine at the U-M Medical School.
Henry will present the initial results of the study Dec. 11 at the 33rd Annual San Antonio Breast Cancer Symposium.
The study looked at the drug duloxetine, or Cymbalta, which is used to treat depression and generalized anxiety disorder. It's also been shown to work in multiple other chronic pain conditions, such as fibromyalgia and, more recently, osteoarthritis. It is believed to decrease pain through its actions in the central nervous system.........
A personalized vaccine is a powerful treatment to prevent recurrence among certain follicular lymphoma patients, as per the latest results of ongoing research led by the University of Pennsylvania School of Medicine. The new findings show that when these patients whose tumors are marked by a specific protein that appears to be present in up to half of people with this type of cancer -- receive a vaccine made from their own tumor cells, disease-free survival is improved by nearly two years, compared with patients who receive a placebo. Based on the new analysis, the team thinks they can explain why the results of prior trials of similar therapeutic cancer vaccines were not as strong as expected.
"The therapy effect of the personalized vaccine is stunning in our trial," says Stephen J. Schuster, MD, an associate professor in the division of Hematology-Oncology and director of the Lymphoma Program at Penn's Abramson Cancer Center. Schuster will present data from a randomized, double-blind, phase III multicenter clinical trial on Monday, Dec. 6 at the annual meeting of the American Society of Hematology (ASH). "Our work stands to revolutionize the approach to personalized vaccine development in lymphoma, and bring new hope to patients who are diagnosed with all types of the disease. This is paradigm changing," Schuster says.........
The genes we possess not only determine the color of our eyes and hair and how our bodies grow, they might also influence the changes that occur in tumors when we develop cancer.
A study by scientists at the Ohio State University Comprehensive Cancer Center-Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC - James) suggests that our normal genetic background - the genetic variations that we inherit - contributes to the kinds of DNA changes that occur in tumor cells as cancer develops.
The scientists compared multiple independent tumors from people with a form of skin cancer called squamous cell carcinoma (SCC) for losses and gains of DNA in tumor cells. They observed that the pattern of these changes is quite similar in tumors from the same person but quite different in tumors from different individuals.
Experiments with an artificial stomach suggest that a popular lemon-lime soft drink could play an unexpected role in improving the effectiveness of an oral anticancer drug. The experiments produced evidence that patients will absorb more of the unnamed drug, tested in Phase I in clinical trials, when taken with "flat" or degassed Sprite. The study appears in ACS' Molecular Pharmaceutics, a bi-monthly journal.
Faraj Atassi and his colleagues note that efforts are underway to develop more anticancer medications that patients can take by mouth. However, biological variations among patients due to variations in stomach acidity and other factors can reduce the effectiveness of oral anticancer drugs. Such was the case with the unnamed anticancer drug in the study, identified only as "Compound X." There were wide differences in how the drug was absorbed in the first patients who took it.
The researchers combined Compound X with Captisol, a substance that helps improve the solubility of drug ingredients, and turned to the artificial stomach. That glass-and-plastic device is used to study how drugs and foods dissolve through the GI tract. They showed that Sprite seemed to control stomach acidity in a way likely to allow greater absorption of the drug into the body. Based on the results, the researchers suggest that patients in future clinical trials take the drug with Sprite.........
Patients with cancer who experience pain or depression also have a high rate of physical symptoms, such as fatigue, dry mouth and nausea, as per a report in the October 11 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
Having a number of physical, or somatic, symptoms is known to adversely affect patients in primary care settings and those with chronic medical conditions other than cancer, as per background information in the article. "Somatic symptoms account for more than half of all general medical visits, lack a definitive medical explanation one-third to half of the time and are frequently persistent," the authors write. "Physical and psychological factors seem to contribute to somatic symptom reporting, even in patients with chronic medical disorders. These symptoms are linked to substantial functional impairment, disability and health care use, even after controlling for medical and psychiatric comorbidity".
Kurt Kroenke, M.D., of the Richard Roudebush VA Medical Center, Indiana University, and Regenstrief Institute Inc., Indianapolis, and his colleagues analyzed data from 405 patients with cancer who also had either pain or depression. Participants reported the presence and burden of 22 different somatic symptoms, along with the number of days of disability within the prior three-month period and health care use.........
Research published in the recent issue of The Journal of Nuclear Medicine (JNM) shows that a molecular imaging technique may prove useful in early evaluation of therapy response for cisplatin-resistant ovary cancer.
"One of the most promising aspects of molecular imaging is its potential capacity to measure treatment effects long before changes in the tumor size and shape are detected," said Marijke De Saint-Hubert, medical scientist in the Department of Nuclear Medicine at the University Hospital Gasthuisberg, Leuven, Belgium, and one of the authors on an invited perspective article in JNM that comments on the study. It is important to identify response to treatment as early as possible so that ineffective therapies can be discontinued. Patients who are not responding to a given treatment appears to be suffering from unnecessary side effects and may also be offered potentially more effective therapys.
The chemotherapy drug cisplatin is often effective against ovary cancer when first given; however, tumors can become resistant to the drug and start growing again, so the need for second-line therapies is pressing. One potential way to overcome cisplatin resistance is to target the mammalian target of rapamycin (mTOR) pathway. The aim of the study was to evaluate the ability of 18F-FLT, a PET probe for cell proliferation, to predict early response to everolimus (an mTOR inhibitor) in a mouse model of subcutaneously transplanted human cisplatin-resistant ovary cancer.........
A study led by scientists at the University of California, San Diego shows that California's 40 year-long tobacco control program has resulted in lung cancer rates that are nearly 25 percent lower than other states.
"The consistency in the trends from cigarette sales and population surveys was reassuring" said John P. Pierce, PhD, Sam M. Walton Professor of Cancer Research in the Department of Family and Preventive Medicine at UCSD School of Medicine and director of the Population Sciences Division at Moores UCSD Cancer Center. "What is really important is that the widening gap in smoking behavior between California and the rest of the nation is replicated in the lung cancer data 16 years later. There is no other behavior that affects a disease like this".
California established the nation's first comprehensive Tobacco Control Program in 1989. Subsequently, the rate at which Californians reduced smoking doubled. Californians now smoke half as a number of cigarettes as people in the rest of the country (9.3 percent/17.8 percent), and fewer than 10 percent of its population smokes, as per a research studyreported in the journal Cancer Epidemiology, Biomarkers and Prevention. The study credits the state's aggressive tax on cigarettes and its decades-long, comprehensive tobacco control program.........
A consortium of cancer scientists has identified four chromosome locations with genetic changes that are likely to alter a woman's risk of developing ovary cancer. The findings are published in Nature Genetics in an article authored by a Mayo Clinic researcher.
Scientists say that while more needs to be learned about the function of the specific chromosomal regions involved in susceptibility, the discoveries move them a major step closer to individualized risk evaluations for ovary cancer. In the future, women at greatest risk due to these and other inherited changes appears to be offered increased surveillance or preventive measures.
"In searching the genome, we came up with some surprises on chromosomes 2, 3, and 17," says Ellen Goode, Ph.D., Mayo Clinic genetic epidemiologist and main author. "While examining the usual suspects in a region on chromosome 8, we observed that SNPs linked to ovary cancer risk were located quite a distance away from those linked to risk of other cancers, which suggest that they may act through a different mechanism." SNPs, single nucleotide polymorphisms, are common genetic variants associated, in this case, with cancer risk.
The findings come from a large genome-wide association study (GWAS) that spanned three continents. Following an initial study in over 1,700 cases, the scientists followed up with a study of over 24,000 women. They narrowed the focus to nine regions and confirmed that three loci (locations on the chromosome) were much stronger than the others and a fourth "approached genome-wide significance." These particular loci are linked to serous ovary cancer, the most aggressive and common of the four main types of the disease.........
Chemotherapy, while an effective cancer therapy, also brings debilitating side effects such as nausea, liver toxicity and a battered immune system.
Now, a new way to deliver this life-saving treatment to cancer patients - getting straight to the source of the disease - has been invented by Dr. Dan Peer of Tel Aviv University's Department of Cell Research and Immunology and the Center for Nano Science and Nano Technology together with Prof. Rimona Margalit of the Department of Biochemistry and Molecular Biology.
Drs. Peer and Margalit have developed a nano-sized vehicle with the ability to deliver chemotherapy drugs directly into cancer cells while avoiding interaction with healthy cells, increasing the efficiency of chemotherapeutic therapy while reducing its side effects.
"The vehicle is very similar to a cluster bomb," explains Dr. Peer. Inside the nano-vehicle itself are tiny particles of chemotherapy drugs. When the delivery vehicle comes into contact with cancer cells, it releases the chemotherapeutic payload directly into the cell. As per Dr. Peer, the nanomedical device can be used to treat a number of different types of cancer, including lung, blood, colon, breast, ovarian, pancreatic, and even several types of brain cancers.
Their technological breakthrough was recently published in the journal Biomaterials.........
This is an MRI image of prostate gland, with red regions indicating high-grade prostate cancer based on Rutgers image analysis techniques. The area inside the white outline was confirmed as high-grade cancer by analyzing surgically removed gland.
Credit: Rutgers, UCSF
Rutgers scientists are in the process of developing methods that can accurately assess the severity of prostate cancer by analyzing magnetic resonance images and spectra of a patient's prostate gland. This may help physicians decide more confidently which patients need aggressive therapy and which are better served by "watchful waiting," and could even postpone or eliminate invasive biopsies in patients with low-grade tumors.
In a presentation next month at the world's premier medical image analysis conference, Rutgers biomedical engineers will report that they achieved over 90% accuracy in distinguishing low-grade from high-grade prostate cancers by running computer analyses of the images and spectra made on 19 patients in an early research study.
"The breakthrough we've had in the last few months is that we see image signatures that distinguish aggressive cancers from less aggressive ones," said Anant Madabhushi, associate professor of biomedical engineering at Rutgers and a member of The Cancer Institute of New Jersey (CINJ).
These studies build on earlier research at Rutgers and elsewhere to identify prostate cancer using powerful, high-resolution magnetic resonance imaging (MRI) technology.
"Now we're getting beyond merely identifying whether a person has cancer or not," he said. "This could lead to better patient management and cost savings".........
High-risk prostate cancer and bone mineral content loss
Men with prostate cancer lose significantly less bone mineral content (BMC) as they age than men who are free of the disease, as per research in the recent issue of BJUI The findings are important because loss of BMC can play a key role in the development of fragile bones, fractures and osteoporosis.
American scientists studied 519 participants who joined the Baltimore Longitudinal Study at an average age of 56 between 1973 and 1984. The maximum follow-up was 35 years and the median was 22 years. Seventy-six men who participated in the study were later diagnosed with prostate cancer, with just under a quarter (24 per cent) falling into the high-risk category.
When they charted the individual BMCs of the study subjects over an extended period, the scientists could clearly see that the decline was much larger in healthy men than in men later diagnosed with prostate cancer, particularly those with high-risk prostate cancer. This occurred despite the fact that the initial baseline readings were very similar for all three groups.
The scientists also adjusted the figures to take account of other factors that affect BMC, such as smoking status, body mass index, dietary calcium and vitamin D. However, this did not change the significant differences between the healthy men and those with prostate cancer.........
In its early stages, prostate cancer requires androgens (hormones that promote the development and maintenance of male sex characteristics) for growth, and current first-line therapies target the receptor for these hormones to slow cancer's development and spread.
However, advanced prostate cancers are often androgen-independent, meaning that androgen-blocking therapies are ineffective.
Researchers aren't sure how this shift occurs as prostate cancer advances. One idea is that prostate cancer cells acquire the ability to make their own androgen. Another says that the androgen receptor that is known to stimulate tumor growth can still be active even when the hormone is not present. Most likely, both are important.
A recent study by UNC researchers, reported in the Journal of Biological Chemistry, provides evidence for the second theory, demonstrating that expression of one of a group of genes found only in humans and non-human primates can promote androgen receptor activity in concert with other proteins called coregulators.
One of a group of MAGE genes, so named because they were originally identified in melanoma, called MAGE-11 interacts with another protein, called p300, to provide the cancer cells with a way to enhance androgen receptor signaling and promote tumor growth, even when patients are undergoing androgen deprivation treatment.........
Radical cuts to social welfare spending to reduce budget deficits could cause not just economic pain but cost lives, warn experts as per a research findings published on bmj.com today.
While there is a major debate under way about the potential economic impacts of radical budget cuts in Europe, David Stuckler from the University of Oxford and colleagues dissect the effect of public spending on people's health.
Their analysis shows that levels of social spending in Europe are "strongly associated" with risks of death, particularly from diseases relating to social circumstances, such as heart attacks and alcohol-induced illness.
As such, they argue that, eventhough governments may feel they are protecting health by safeguarding healthcare budgets, social welfare spending is as important, if not moreso, for population health.
The team reviewed data on social welfare spending collected by the Organisation for Economic Cooperation and Development (OECD) from 15 European countries in the years 1980 to 2005. This includes programmes to provide support to families and children, help the unemployed obtain jobs, and support for people with disabilities, all of which could plausibly affect health.
They analysed the relationship between trends in these data and social spending. They observed that when social spending was high, mortality rates fell, but when they were low, mortality rates rose substantially.........
Colorectal cancer, cancer of the colon and rectum, is a common cause of mortality worldwide. Statistical data showed that the number of deaths caused by colorectal cancer is increasing in both men and women. Proteins are functional components of the cell that regulate the cell's activity. Understanding the differential expression of proteins in colorectal cancer and normal tissues will lead to a better understanding of the development of the disease, furthermore, these proteins may serve as biomarkers for therapy or detection of the disease. Hydrophobic proteins play a vital role in various cellular processes, by virtue of their cellular location, and may serve as a target for drug-targeted treatment.
This study, led by Assoc. Prof. Dr. Gam Lay Harn from Universiti Sains Malaysia, Malaysia will be published on June 14, 2010 in the World Journal of Gastroenterology By using two-dimensional gel electrophoresis (2D-PAGE), the hydrophobic proteins extracted from colorectal cancer tissues were separated as per their pI and MW, subsequently the protein profiles between malignant and normal tissues were compared. Using this approach, the scientists identified a few differentially expressed proteins that were up-regulated in malignant tissues. The expression of such proteins was shown to be significantly correlation to stage and grade of the cancer and also to gender of the patients.........
Stephanie Fraley, a doctoral student in chemical and biomolecular engineering, was lead author of the study. Photo by Will Kirk/HomewoodPhoto.jhu.edu
Showing movies in 3-D has produced a box-office bonanza in recent months. Could viewing cell behavior in three dimensions lead to important advances in cancer research? A newly released study led by Johns Hopkins University engineers indicates it may happen. Looking at cells in 3-D, the team members concluded, yields more accurate information that could help develop drugs to prevent cancer's spread.
The study, a collaboration with scientists at Washington University in St. Louis, appears in the recent issue of Nature Cell Biology.
"Finding out how cells move and stick to surfaces is critical to our understanding of cancer and other diseases. But most of what we know about these behaviors has been learned in the 2-D environment of Petri dishes," said Denis Wirtz, director of the Johns Hopkins Engineering in Oncology Center and principal investigator of the study. "Our study demonstrates for the first time that the way cells move inside a three-dimensional environment, such as the human body, is fundamentally different from the behavior we've seen in conventional flat lab dishes. It's both qualitatively and quantitatively different".
One implication of this discovery is that the results produced by a common high-speed method of screening drugs to prevent cell migration on flat substrates are, at best, misleading, said Wirtz, who also is the Theophilus H. Smoot Professor of Chemical and Biomolecular Engineering at Johns Hopkins. This is important because cell movement is correlation to the spread of cancer, Wirtz said. "Our study identified possible targets to dramatically slow down cell invasion in a three-dimensional matrix".........
Virginia Commonwealth University scientists have discovered a mechanism by which an enzyme regulates gene expression and growth in melanoma cells, a finding that could someday lead to more effective drugs to attack cancers and make them more treatable.
Melanoma, the most serious type of skin cancer, is highly resistant to current therapeutic strategies for reasons that are not well understood. New research at VCU suggests that an enzyme discovered in 2003 might be used to target a specific genetic component that helps to regulate gene expression and defends melanoma cells against therapy.
The findings are reported online this week in the Proceedings of the National Academy of Sciences.
"By selectively and specifically targeting molecules for degradation that serve as gatekeepers for cancer growth, progression and resistance to treatment, it appears to be possible to turn the cancer cells' defense into an offense that can be used as an effective approach to destroy the tumor," said Paul B. Fisher, Ph.D., professor and chair of the Department of Human and Molecular Genetics and director of the VCU Institute of Molecular Medicine in the VCU School of Medicine.
Several years ago, Fisher led a team of researchers at Columbia University in identifying an enzyme involved in halting the growth of human cancerous melanoma and other cancer cells. The enzyme, called human polynucleotide phosphorylase or hPNPaseold-35, drives malignant cells to irreversibly lose their growth potential and acquire properties of more normal cells, a process called terminal cell differentiation. The enzyme also is important in cellular senescence, when a cell cannot divide anymore and dies. Additionally, the researchers developed new strategies for promoting cancer cell-specific expression of this enzyme, which reduced tumor growth in animal cancer models.........
